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ANTIDYSRHYTHIMC Flashcards

1
Q

Phase 0 of the myocytes

A

rapid depolarization (influx of Na due to opening of fast Na channels)

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2
Q

Phase I of the myocytes

A

partial repolarization inward Na current deactivated, outflow of K

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3
Q

Phase 2 of the myocytes

A

Plateau (slow inward of Ca2+ balanced by outward K+ current)

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4
Q

Phase 3 of the myocytes

A

repolarization (calcium current inactivates, K+ outflow)

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5
Q

Phase 4 of the myocytes

A

Resting membrane potential (Na+ efflux and K+ influx via Na+/K+ ATPase pump)

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6
Q

Absolute Refractory period

A

Phase 0-2 & early part of 3, time period where the cell can not depolarize agin

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7
Q

Cardiac myocytes

A

Fast response

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8
Q

Class I agents works on which phase?

A

Works on phase 0

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9
Q

Class II and IV works on which phase?

A

Phase 2

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10
Q

Class III and I A works

A

Phase 3

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11
Q

Phase 2 drugs are classes

A

Acts on Class II and IV

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12
Q

Phase 3 drugs are classes

A

Acts on Class III and IA

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13
Q

****Cardiac nodal tissue’s (SA & AV node)

depolarization is largely controlled by

A

Ca2+ channel current and are referred to as slow response tissue

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14
Q

Phases of action potential of cardiac

pacemaker (nodal) cells

A 
Phase 4	spontaneous	depolarization	to	threshold	(also	called	diastolic	depolarization	or	
pacemaker	potential)	–	diffusion	of	
K+	out	of	cell	decreases	
progressively	and	diffusion	of	Na+
into	cell	increases	progressively.		
During	the	last	1/3rd	of	phase	4,	
Ca2+	ions	begin	to	diffuse	into	the	
cell	
• Phase 0 slow depolarization Ca2+
diffuses into the	cell	and	slight Na+
influx	
• Phase 3 repolarization –K+ diffuses out of	the cell	
• Pacemaker cells are slow response	tissue
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15
Q

Are the sodium channels the same for the pacemaker nodal cells?

A

NO

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16
Q

PACEMAKER OF MUSCLE CELLS

A

SLOW RESPONSE TISSUE WHEN COMPARED TO MYOCYTE CELLS (BECAUSE THEY DON’T CONDUCT ion movements as fast)

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17
Q

Cardiac antidysrhythmic drugs produce their pharmacologic effects by:

A

blocking the passage of ions across Na+, K+, and/or Ca2+ ion channels present in the heart

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18
Q

Drugs may decrease automaticity (meaning these agents will slow “automatic” rhythms) by altering any of the 4
determinants of the spontaneous pacemaker discharge

A
  1. Decrease phase 4 depolarization
  2. Increase threshold potential
  3. Increase maximum diastolic potential
  4. Increase action potential duration
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19
Q

*****Vaughan-Williams Classification of

Antiarrhythmic Drugs

A
  1. Class I- Na+ Channel Blockers (fast Na only)
  2. Class II- Beta-adrenergic Blockers
  3. Class III - K+ Channel Blockers
  4. Class IV - Ca2+ Channel Blockers (only VERAPAMIL and DILTIAZEM
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20
Q

***Class IA Names

A

– Quinidine (PDQ)
– Procainamide
– Disopyramide

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21
Q

**Class II Names

A

Esmolol (MEPA)
Acebutalol,
Propranolol,
Metoprolol

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22
Q

*** Class III Names

A 
- Amiodarone	(ADIDS)
– Dronedarone		
– Dofetilide
– Ibutilide	
– Sotalol
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23
Q

***Class IB Names

A

– Lidocaine (LPM)
– Mexiletine
– Phenytoin

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24
Q

***Class IC Names

A

– Flecainide (FP)

– Propafenone

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25
Q

***Class IV Names

A

– Verapamil

– Diltiazem

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26
Q

The following agents are also anti-arrhythmic drugs but do

not fit into the Vaughan-Williams Classification system

A

Digoxin (DAMI)
– Adenosine
– Magnesium
– Ivabradine (Corlanor)

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27
Q

Class I agents are classified as Na+ channel blockers (fast Na+ channels)

A

• Class I anti-arrhythmic drugs bind to and block/inhibit fast Na+ channels that are responsible for the rapid depolarization (phase 0) in non-nodal tissue, which results in the following:
– Inhibits depolarization by reducing the rate of rise of phase 0 of the action potential, also known as Vmax (aka: Decreases phase 0 of the fast action potential) and decreases the amplitude of the cardiac action potential
– Slows conduction velocity in atria, ventricles and His-Purkinje fibers (non-nodal tissue)
– Decreases automaticity

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28
Q

Antidysrhythmic effects are due to blockade of the responses
of beta-adrenergic receptors in the heart to SNS stimulation, as
well as the effects of circulating catecholamines

A
  • Class II drugs are beta-adrenergic antagonists

* Every beta-blocker on the market is a Class II agent!

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29
Q

Class II mechanism of action (NODAL)

A

Decrease automaticity by decreasing the rate of phase 4 spontaneous depolarization of SA node.
Decrease AV nodal conduction velocity
Negative chronotrophic
Negative Inotrope (decrease phase II of non-nodal tissue
Can produce AV block

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30
Q

Class III agents are classified as

A

K+ channel blockers.

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31
Q

Class III antiarrhytmic drugs bind to and blcok

A

K+ ion channels which prolong repolarization (phase III) by :
prolonging the duration of the cardiac action potential and the effective refractory period (ERP) (prolong refractoriness) of atrial and ventricular myocytes

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32
Q

Class IV: Mechanism of action (MYOCYTES)

A

Verapamil and diltiazem act by inhbiting the influx of Ca2ions acrross slow L-type voltage-gated ca2+ channels of CARDIAR MYOCYTES, SA and AV nodal
So they are NEGATIVE INOTROPE.
NEVER GIVEN TO Heart failure with Decreased EF (HfrEF)

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33
Q

Class IV agents increase the (in NODAL)

A

Threshold voltage resulting in decreased amount of Ca2+ entry into the nodal cell.
Took longer for phase IV to reach

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34
Q

**Class IV mechanism of action (NODAL)

A

Inhibiting calcium entry into the cardiac NODAL tissue cells results in :

  1. Decreased rate of spontaneous phase 4 depolarization
  2. Decreased SA and AV node automaticity
  3. Decreased Conduction velocity through AV node (negative dromotrope)–>Prolonged PR
  4. Decrease HR
  5. Increased Refractory Period.
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35
Q

Class IV agents : effects of only those 2 drugs, but NOT a class IV mechanism

A

Inhibits calcium entry into vascular smooth muscle tissue which results in relaxation of vascular smooth muscle of coronary arteries and systemic arteries (HYPOTENSION mechanism)

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36
Q

Useful in reentrant tachycardia that arise from or use the SA and AV nodes

A

Verapamil and Diltiazem

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37
Q

Class I - Na+ Channel Blockers

Another difference:

A 
All class I agents have a predominant affinity for a particular state of the Na + channels when they block the Na+ channel, which influences its clinical effects
- Affinity during activation and/or inactivation.
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38
Q

All Class I agents possess a

A

property called rate dependence (used dependence), their sodium channels are best at fast HR

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39
Q

Na+ Channel blockade and slowing of conduction by the drugs is

A

GREATEST at fast heart rates and least during Bradycardia.

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40
Q

Sodium channel blockers work better

A

when HR is higher.

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41
Q

Which category Class IA agents:

A

All class IA In addition to blocking fast Na+ channels ALSO block K+ channels in the heart.
They have Class I and Class III effects.
Non-nodal tissues

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42
Q 
All class IA agents have proarrythmic agents: By blocking \_\_\_\_\_\_\_\_they do what? putting patient at risk for \_\_\_\_\_\_\_
Significant \_\_\_\_\_\_ \_\_\_\_\_
A

blocking potassium Channels( prolonged QT ) Increase Torsades de pointes
Significant negative inotropes.

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43
Q

Class IA drugs are broad spectrum agentst and are effective for both

A

SVTs and Vtach

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44
Q

**Class ____are rarely used for anesthesia due to ______ ______

A

Profound HYPOTENSION

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45
Q

Quinidine Class IA

A 
is a class IA agents that blocks Na+ channels in the "open' state only AND also blocks K+ currents/channels
Posess alpha adrenergic ANTAGONIST, anticholinergic effecfs and ANTIMALARIAL EFFECTS
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46
Q

Clinical use of Quinidine first slide not important.

A

Last resorts for Atrial or ventricular arrhythmias

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47
Q

Additional pharmacological effects

A

Prolong QRS and *****QT interval

Shortened PR

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48
Q

Metabolism of Quinidine

A

metabolize in liver via CYP3A4
active metabolites
HIGHLY PROTEIN BIND to ALBUMIN80-90
20% Kidney as unchanged drug.

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49
Q

Avoid quinidine in

A

HF patients

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50
Q

Quinidine SIDE EFFECTS

A 
*****Diarrhea (most common) 
Nausea
Syncope
HYPOTENSION
REFLEX TACHYCARDIA
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51
Q

Quinidine Immunological reactions

A

LUPUS-LIKE REACTIONS

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52
Q

Cinchonism with ________include

A

Quinidine; tinnitus, headache, decreased hearing acuity, blurring vision

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53
Q

*****Quinidine -Drug interactions

A

**Potentiates/ACCENTUATES non-depolarizing and depolarizing neuromuscular blockers.

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54
Q

Quinidine increases ______serum concentration.

A

digoxin

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55
Q

Decrease quinidine concentration

A

CYP 3A4 inducers

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56
Q

INcrease quinidine concentration

A

CYP3A4 inhibitors

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57
Q

Quinidine has a ______adrenergic antagonists which can produce _______-

A

alpha; Vasodilation.

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58
Q

PROCAINAMIDE is a ________ and it

A

Class IA ; blocks Na+ channels in the open state and ALSO blocks K+ current/channels, and has a VERY WEAK anticholinergic effects. Same electrophysiologic

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59
Q

Clinical use of Procainamide

A

Does same as quinidine except does not have ANTAGONISTIC PROPERTIES

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60
Q

PROCAINAMIDE Dosing

A

In urgent situation for VTACH conversion

100mg IV every 5 minutes until 15mg/kg given, the arrhythmia ceases OR the QRS widens >50%

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61
Q

Procainamide Afib concersion

A

Gram IV OVER 30 minutes, then 2mg/min

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62
Q

Procainamide is eliminated by both

A

Renal metabolism and

hepatic metabolism

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63
Q

**Acetylation of procainamide produces an

A

***active metabolite called NAPA (N-Acetyl procainamide)

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64
Q

The activity of N-actetyl transferase enzyme is

A

determined genetically, patients may either have

-normal activity or reduced activity (slow acetylators) or increased activity (Fast acetylators)

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65
Q

Procainamide clearance required_______

A

required adequate kidney

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66
Q

Both procainamie and NAPA are excreted via the kidneys necessating

A

dosage adjustements in renal failure patietn.

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67
Q

NAPA

A

has class III effects and prolonged the half life.

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68
Q

No oral dose of

A

Procainamide

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69
Q

**BIGGEST CONCERN FOR ANESTHESIA as far as procainamide

A

*****HYPOTENSION

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70
Q

Rapid IV administration of procainamide can lead to hypotension which limits

A

the use of this agents during general anesthesia
– Hypotension is due to direct myocardial depressive effect
– Never give as a rapid IV bolus

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71
Q

Procainamide not given in patients with

A

heart block –> can lead to systole

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72
Q

Oral dosage form of procainamide

A

NO LONGER AVAILABLE in the USA.

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73
Q

Increased effect of nondepolarizing and depolarizing

A

With procainamide

74
Q

Disopyramide (will never give as anesthesia providers)

A

possess Na+ channel blockade, K+ channel blockade and has very potent ANTICHOLINERGIC effects

75
Q

Most potent class I agents with anticholinergic effects

A

DISOPYRAMIDE

76
Q

Most serious side effect of DISOPYRAMIDE

A

Tachycardia
Dry mouth
URINARY RETENTION

77
Q

Class I B Agents

A

lidocaine
Mexiletine
Phenytoin

78
Q

Class IB agents action

A

Less potent Na+ Channel blocks (fast sodium channels) compared to Class IA and IC agents, they produce little effect on shortening Vmax and slowing conduction compared to other class I agents.

79
Q

Class IB agents decrease the effective refactroy period

A

Shortens refractoriness and shorten the action potential duration in normal cardiac ventricular muscle. UNLIKE IA and IC agents.

80
Q

**Class IB agents decrease the effective refractory period

A

***Shortens refractoriness and shorten the action potential duration in normal cardiac ventricular muscle. UNLIKE IA and IC agents.

81
Q

Lidocaine is a ______Agents

A

is a local anesthetist agent and used in the acute IV treatment of ventricular arrhythmias ONLY

82
Q

Lidocaine: Particular useful in suppresing

A

re-entry arrhythmias ; NOT USEFUL in ATRIAL ARRYTHMIAS

83
Q

In patients with noram CO, hepatic function and hapetic blood flow

A

giv In patients with normal cardiac output, hepatic function,
and hepatic blood flow, lidocaine 2mg/kg followed by
continuous infusion of 1 to 4 mg/min should provide
therapeutic drug levels

84
Q

Lidocaine causes (advantages over procainamide and quinidine)

A

FAR LESS HYPOTENSION

Less cardiovascular adverse effects.

85
Q

LIDOCAINE On heart conduction:

Can you use for HF patients

A

Improves AV conduction
• Action potential duration and effective refractory period
is shortened
- yes

86
Q

• Pulseless VT/VF Conversion or VT with a pulse

If LVEF < 40%

A

1 -1.5 mg/kg IV bolus; repeat 0.5-0.75 mg/kg q 3-5 minutes (Maximum of 3mg/kg) If LVEF <40% give 0.5-0.75mg/kg

• VT Maintenance
– 1-4 mg/MINUTE via continuous IV infusion

87
Q
  • *** LIDOCAINE METABOLISM

* *** on anesthesia.

A

*****Because of the rapid rate at which lidocaine is metabolized in the liver, any condition that decreases cardiac output or
decrease liver blood flow can decrease lidocaine clearance and increase risk for toxicity
• Anesthesia, acute MI, congestive heart failure, shock or certain surgical procedures can decrease cardiac output and/
or decrease liver blood flow

88
Q

Lidocaine adverse reaction principal reaction

A

CNS **stimulation symptoms: SEIZURES, NYGSTAGMUS

When lidocaine is greater than 5 mcg/ml

89
Q

Lidocaine does what on cardiac contractility?

A

decreases far less than any other antiarrhythmic used

90
Q

Lidocaine toxication can lead to e

A

HYPOTENSION

PERIPHERAL VASODILATION.

91
Q

LIDOCAINE Threshold for seizure is decreased with

A

Arterial hypoxemia
HYPERKALEMIA
ACIDOSIS
emphasizing the importance of monitoring these parameters during continuous IV lidocaine.

92
Q

• Beta-blockers such as propranolol or cimetidine (Not used IV anymore)

A

– May reduce hepatic blood flow & thus decrease lidocaine
clearance which can increase lidocaine blood levels and the
increase incidence of adverse reactions, including CNS
adverse effects such as seizures

93
Q

**Mexiletine

A

s an orally active amine analog of lidocaine
– Mexiletine has been structurally modified to reduce
first-pass hepatic metabolism and permit chronic oral
therapy

94
Q

Does everything lidocaine does but is PO

A

Mexelitine

95
Q

Phenytoin mechanism of action: same as lidocaine

A

The effects of automaticity and conduction velocity are similar to lidocaine
Slow the rate of recovery of voltage activateted Na+ ions from inactivation
Shortens QT

96
Q

Phenytoin exhibits _______pharmacokinetics which is a type of

A

Michaelis-Mentin pharmacokinetics,

which is a type of non-linear pharmacokinetics where phenytoin’s metabolism is saturable

97
Q

Clinical Use of Phenytoin
– Suppression of ventricular dysrhythmias.
– Rarely used anymore, used primarily as an anticonvulsant
Dose______
– Note: will precipitate with D5W; use normal saline only
– Max infusion rate is 50 mg/min, infusing faster than this
can cause profound myocardial depression
• Will be reviewed later in more detail with anticonvulsant
medication

A

Suppression of ventricular dysrhythmias (VTach and Tdp)
Dose: 100 mg IV q 5 minutes (1.5 mg/kg) or 10 to 15 mg/
kg (1000 mg max) has been given

98
Q

*****Max infusion rate is _____mg/min, infusing faster than this can cause_______

A

50 mg/min, profound myocardial depression

99
Q

Class IC agents are the most ________

A

POTENT ARRHYTHMIC AGENTS at slowing CONDUCTION VELOCITY of the cardiac impulse and decreasing the rate of phase 0 depolarization> they dissociate slowly from the Na channels.

100
Q

Class IC agents are ABSOLUTELY CONTRATINDICATED in
patients with structural heart disease (i.e.: previous MI)
due to increased mortality rates in these types of
patients which was based on results of the CAST trial

A

In
patients with structural heart disease (i.e.: previous MI)
due to increased mortality rates in these types of
patients which was based on results of the CAST trial

101
Q

**PROPAFENONE Class IC

A

*****– Also has weak beta-blocker properties since it is structurally
similar to beta-blockers
– Also posseses calcium-channel blocking effects

102
Q

****Propafenone is extensively metabolized in the

A

Metabolized extensively in liver by CYP 450
– Follows nonlinear pharmacokinetics
– Has pharmacologically active metabolites

103
Q

Not given in BRONCHOSPASMS patients.

A

Non-selective beta blocks

104
Q

A structural analog of thyroid hormone (thyroxine)

A

Amiodarone is highly lipophilic, is concentrated in many tissues and is eliminated extremely slowly

105
Q

Amiodarone Mechanism of action

A

– K+ channel blockade (Class III)
– Na+ channel blockade of inactivated state (Class I)
– Non-selective beta-blocking properties (Class II)
– Some Ca2+ channel blockade activity (Class IV)
– Amiodarone possesses electrophysiologic characteristics from all 4
Vaughan Williams classes
– Also blocks alpha-adrenergic receptors

106
Q

****Amiodarone Mechanism of action

A

– K+ channel blockade (Class III)
– Na+ channel blockade of inactivated state (Class I)
– Non-selective beta-blocking properties (Class II)
– Some Ca2+ channel blockade activity (Class IV)
*****Amiodarone possesses electrophysiologic characteristics from all 4
Vaughan Williams classes
– Also blocks alpha-adrenergic receptors

107
Q

**Amiodarone possesses

A

Amiodarone possesses electrophysiologic characteristics from all 4
Vaughan Williams classes

108
Q

Although amiodarone prolongs the QT interval, its use is associated with a lower incidence to TdP than Class 1A and other Class III agents
– TdP is the most common arrhythmia seen with amiodarone
use (proarrhythmic agent)
• Dosage adjustments are not required in hepatic, renal or
cardiac dysfunction

A

PROARRHYTHMIC agent

Rare Torsades de pointes.

109
Q

Clinical uses for Amiodarone

A

Used for every known arrrhtymias, above or in ventricles.

110
Q

Onset of action with amiodarone

A

onset : 8-24 months

Peak effect: 1 week to 5 months

111
Q

Amiodarone to

A

Concentrated in many tissues

HIGH Vd

112
Q

Duration of effect after discontinuation

A

7-50 days because of LARGE

113
Q

Half life of amiodarone

A

LONG , nobody know about 40 days

114
Q

AMIODARONE can still be use in

A

liver failure.

115
Q

Can you dialize amiodarone

116
Q

*****The most serious adverse effect during CHRONIC AMIODARONE therapy is

A

**PULMONARY FIBROSIS, which can be fatal.

117
Q

Screening test such as : 4 tests NEEDED For amiodarone therapy.

A

CXray
Pulmonary function tests
Thyroid panel
Liver fuction s

118
Q

3 top considerations for amiodarone.

A

High volume of distribution
long half life
Pulmonary fibrosis

119
Q

***ANESTHESIA considerations for amiodarone

A

lowest O2 concentration possible during anesthetic delivery to prevent the formation of free O2 radicals.

120
Q

***2 distinct types of presentation of amiodarone pulmonary toxicity

A

EALRY ONSET PULMONARY TOXICITY

PULMONARY ALVEOLITIS

121
Q

Amiadarone major cardiac

A

AV blocks
HYPOTENSION< HYPOTENSION
Prolong QT interval

122
Q

Amiodarone recommended over

A

PROCAINAMIDE

123
Q

Can be safely administered in HF

A

Amiodarone.

124
Q

Amiodarone Thyroid toxicity

A

Contains 2 iodine molecules –> Can inhibits the conversion of T4 to T3 can cause HYPO or HYPERTHYROIDISM

125
Q

Patient on Amiodarone preop

A

Check thyroid and liver

126
Q

Amiodarone eye effects

A

Corneal microdeposits.

127
Q

Drug to drug interactions amiodarone

A

Numerous

Think about CYP3A4 inducers and inhibitors.

128
Q

Classic CYP3A4 enzymes inhibitors

A

AMIODARONE

129
Q

AMIODARONE can increase

A

Digoxin levels by 50-100%

130
Q

AMIODARONE Can increase level of

A

Procainamide

Quinidine

131
Q

Amiodarone dosing

A

VT/VF pulseless arrect ACLS
300mg/20ml D5W or NS IV push
If VF/pulseless VT recurs, consider 2nd dose 150mg Dose IV push/IO

132
Q

VT/ VF maintenance

A

1mg/min IV infusion x 6 hours then 0.5mg/min x 18 hours

133
Q

Tachycardia other than VT/VF

A

150mg IV over 10 minutes.

Maintenance infusion 1mg/min x 6 hours

134
Q

Sotalol is a (Class ___)
• Mechanism of action
– Inhibits the delayed-rectifier (IKr) current and other K+
currents in cardiac muscle tissue. The K+ channel blockade
is seen at higher dose (>160mg)
– Non-selective beta-adrenergic antagonist at low doses

A

III; Both a nonselective beta-adrenergic antagonists (low doses) and K+ channel blocker
Inhibits the delayed-rectifier (IKr) current and other K+
currents in cardiac muscle tissue. The K+ channel blockade
is seen at higher dose (>160mg)

135
Q

Use of Sotalol

A

• Clinical uses
– Sustained VTach or Vfib
– Maintenance of NSR in symptomatic atrial fib/flutter
• Only available as an oral dosage formulation

136
Q

Sotalol is Supplied as a ______mixture both the I and D are equipotent as

A

Racemic; K+ channel blockers

137
Q

L-enantiomer has more

A

potent beta adrenergic antagonist

than the d-enantimorer.

138
Q

Pharmacologic effect SOTALOL

A

Prolongs the action potential duration (Phase III)
– Prolongs AV refractoriness and action potential duration
– Decreases automaticity
– Slows AV Nodal conduction
– Prolongs the QT interval
– Negative inotrope/chronotrope/dromotrope

139
Q

Sotalol half life is

140
Q

Contraindications of SOTALOL

A

Bronchial asthma, left venticular dystrophy, prolong QT intervals, 2nd and 3rd degree AV blocks
Tordades
HYPOTENSION< BRADYCARDIA

141
Q

Ibutilide

A

inhibits the IKr in cardiac muscle
delayed repolarization
SLOW SODIUM CHANNELS>

142
Q

Ibutilide: Use for the conversion of

A

Conversion of recent onset of atrial fibrillilation

143
Q

All class III agents can cause

A

**TORSADES or other ARRHYTHMIAS

144
Q

Do not study for IBUTILIDE

145
Q

Dofetilide (Tikosyn) is a : CLASS ____agents

A

Pure K+ channel blocker AVAILABLE only in oral dosage form; III prolongs action potential and prolong repolarization

146
Q

Dofetilide mechanism of action

A

Blockade of the cardiac ion channel carrying the rapid component of the delayed rectifier potassium current Ikr **(a pure Ikr blocker) Delayed rectifier

147
Q

Dofetilide Indication (2) : ONLY____

A

1.Conversion of recent onset atrial fibrillation and atrial flutter to NSR
2.Maintenance of NSR for the recently cardioverted patient.
ATRIAL

148
Q

Dofetilide can prolong

A

QT Interval

149
Q

Hospitalization and ______ for a minimum of ____hours

A

ECG monitoring , 72

150
Q

What must be closely monitored: dofetilide.

A

Renal function and QTc

151
Q

Adverse effected of Dofetilide rare

A

Headache
chest pain
Dizziness

152
Q

Warning of Dofetilide

A

Can cause torsades

Maintain normla potassium

153
Q

Halothane and Dofetilide

A

Increased risk of cardiac arrhythmia

154
Q

Dofetilide other drugs can prolong QT interval

A

Phenotiazines,
Haloperidol
Droperinol
Dolasetron.

155
Q

For Dofetilide any drugs that inhibits _______could _______plasma concentration.

A

inhibis CYP3A5 could increased plasma concentration s of dofetilide

156
Q

Any drug that inhibits Renal secretion of dofetilide will _______Plasma concentration

A

Increased Acute tubular secretion process

157
Q

Drug to Drugs interaction: Dofetilide

A

Hypokalemia and HYPOMAGNESEMIA , increasing potential for tornadoes

158
Q

Dronedarone (multaq) is a __________ anti arrhythmic agent that is related to _______and is a _____agent

A

non-iodinated (NO IODINE) anti arrhythmic agent that is structurally related to amiodarone and is a CLASS III AGENT

159
Q

Mechanism of action of dronedareon

A

exhibits properties of all 4 classes of Vaughan william classification
MAIN ANTIARRHYTMI: Potassium channel blockade

160
Q

Metabolism

161
Q

Side effects of dronedarone

162
Q

ANESTHESIA

A

You can’t use any drug prolonging QT interval

163
Q

***Dronedarone contraindicated concomitant use of

A

Phenothiazines

Any drug that PROLONGS QT INTERVALS

164
Q

*****No longer use of DRONEDARONE because

A

Increase risk of death, stroke and HF in decompensated HF or permanent afib

165
Q

MISCELLANEOUS AGENTS

A

Do not fall into the Vaughan William classification.

166
Q

Adenosine is an ______

A

Endogenous purine NUCLEOSIDE in all cells of the body with transient NEGATIVE CHRONOTROPIC and DROMOTROPIC EFFECS on cardiac pacemaker tissues

167
Q

**CLINICAL USE OF ADENOSINE

A
  • Paroxysmal SVT (CONVERSION)

- Not use if they have AFIB

168
Q

**Mechanism of action Adenosine

A

binds to adenosine recepotr
G-protein coupled receptor
Adenosine 1 receptor in SA node and AV node
Activate receptors ACH sensitive K channels that increase activation of outward K+ current leading to hyper polarization of the cell membrane and shortening got action potential duration. I’m

169
Q

**Mechanism of action

A

Increases AV node refractoriness via decreased cAMP and decreasing cAMP induced calcium conductance in slow response tissue (AV node)

170
Q

As a result of the mechanism of adenosine:

A

Slows conduction of cardiac impulses through the AV node (negative dromotrope) and increases AV nodal refractoriness
Slows sinus rate (negative chronotrope)

171
Q

Pharmacokinetisc of Adenosine

A
  1. IV
  2. T 1/2 < 10 seconds
  3. Rapidly cleared from the circulation through CELLULAR UPTAKE MECHANISM primarily ERYTHROCYTES and vascular endothelial cells.
172
Q

Would hepatic and renal failure expected to alter effectiveness of Adenosine

173
Q

Dosing of Adenosine: Dosing and how many minutes apart.

A

6mg IV
12 mg IVP x 2 (3 minutes apart)
Max 30 mg

174
Q

Adverse effects of Adenosine

A

Chest burning tightens due to bronchospasm.

175
Q

***Drugs to drug interactions : Adenosine.

A

METHYLXANTHINE: Theophylline or caffeine are adenosine antagonist. May required a higher dose of adenosine for effectiveness

176
Q

Dipyridamole does what ?

A

(adenosine uptake inhibitor)
Increases effect of adenosine
Blocks cellular uptake mechanism of adenosine.

177
Q

Contraindication of adenosine

A

2nd or 3rd degree HB

178
Q

Ivrabradine (coplanar)

A

oral agent only , HYPERPOLARIZATION ACTIVATED CYCLIC NUCLEOTDIE GATED CHANNEL BLOCKERS
To control HR and keep it down

179
Q

Ivrabradine (coplanar) mechanism of action

A

Slow diastolic depolarization by selectively and specifically inhibiting the If current (funny current) which is responsible for regulating the intrinsic pacementer activity in the SA node, this leads to decreased HR

180
Q

Most common adverse effects: Ivrabradine (coplanar)

A

Brady cardia

Afib

181
Q

Avoid using with Ivrabradine (coplanar)

A

verapamil and diltiazem

will inhibit metabolism of ivabradine. thereby increasing risk of adverse effects such as BRADYCARDIA

SRNAPharmacology I (29 decks)

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